Metabolic acidosis pathophysiology: Difference between revisions

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| [[File:Siren.gif|30px|link=Metabolic acidosis resident survival guide]]|| <br> || <br>
| [[Metabolic acidosis resident survival guide|'''Resident'''<br>'''Survival'''<br>'''Guide''']]
|}
{{Metabolic acidosis}}
{{Metabolic acidosis}}
{{CMG}}
{{CMG}}


==Overview==
==Overview==
==Pathophysiology==
==Pathophysiology==
===Compensatory mechanisms===
Metabolic acidosis is the state of low blood pH that can result from:
* Failure of the kidneys to excrete H+
* Increased H+ load
* Loss of bicarbonate
 
Shown below is a table summarizing the mechanisms of metabolic acidosis.
 
{| style="cellpadding=0; cellspacing= 0; width: 600px;"
|-
| style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align=center |'''Mechanism''' || style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align=center |'''Conditions'''
|-
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |Failure to excrete H+
|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |
''Decreased production of NH4+:''
* Renal failure
* Renal tubular acidosis type 4 (hypoaldosteronism)
''Decreased secretion of H+''
* Renal tubular acidosis type 1
|-
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |Increased H+ load
|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |
* Lactic acidosis
* Ketoacidosis
* Ingestions
* Massive rhabdomyolysis
|-
|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |Loss of bicarbonate
|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |
''Gastrointestinal loss of bicarbonates:''
* Diarrhea
* Cholestyramine
''Renal loss of bicarbonate:''
* Renal tubular acidosis type 2
* Diuretics such as carbonic anhydrase inhibitors)
|-
|}
 
===High Anion Gap Metabolic Acidosis===
High anion gap metabolic acidosis can be caused by one of the following:
* Lactic acidodis
* Ketoacidosis
* Renal failure
* Ingestions
 
====Lactic Acidosis====
 
====Ketoacidosis====
 
====Renal Failure====
 
====Ingestions====
 
===Compensatory Mechanisms===
Metabolic acidosis is either due to increased generation of acid or an inability to generate sufficient bicarbonate. The body regulates the acidity of the blood by four buffering mechanisms.
Metabolic acidosis is either due to increased generation of acid or an inability to generate sufficient bicarbonate. The body regulates the acidity of the blood by four buffering mechanisms.
* [[bicarbonate buffering system]]  
* [[Bicarbonate buffering system]]  
* [[Intracellular]] buffering by absorption of hydrogen atoms by various molecules, including proteins, phosphates and carbonate in bone.
* [[Intracellular]] buffering by absorption of hydrogen atoms by various molecules, including proteins, phosphates and carbonate in bone.
* [[Respiratory compensation]]  
* [[Respiratory compensation]]  
* [[Renal compensation]]
* [[Renal compensation]]
===Respiratory compensation of metabolic acidosis===
 
===Respiratory Compensation of Metabolic Acidosis===
* For 1 meq/L fall of serum HCO3 levels there is a 1.2 mmHg fall in arterial pCO2.
* For 1 meq/L fall of serum HCO3 levels there is a 1.2 mmHg fall in arterial pCO2.
* The respiratory compensation of [[metabolic acidosis]] is fast and begins within half an hour of metabolic acidosis.
* The respiratory compensation of [[metabolic acidosis]] is fast and begins within half an hour of metabolic acidosis.
* In cases where the metabolic acidosis develops slowly, the respiratory compensation occurs simultaneously with the metabolic acidosis.
* In cases where the metabolic acidosis develops slowly, the respiratory compensation occurs simultaneously with the metabolic acidosis.
* The respiratory compensation usually completes within 12 to 24 hours
* The respiratory compensation usually completes within 12 to 24 hours
* A failure to develop adequate respiratory response indicates an acute underlying respiratory diseases, neurologic disease or a very acute development of metabolic acidosis.
* A failure to develop adequate respiratory response indicates an acute underlying respiratory disease, neurologic disease or a very acute development of metabolic acidosis.
* Formula for checking appropriate respiratory compensation to metabolic acidosis include:
* Formula for checking appropriate respiratory compensation to metabolic acidosis include:
** '''Arterial pCO2''' = 1.5 x serum HCO3 + 8 ± 2 ('''Winters’ equation''')
** '''Arterial pCO2''' = 1.5 x serum HCO3<sup>-</sup> + 8 ± 2 ([[Winters' formula]])
** Arterial pCO2 = Serum HCO3 + 15
** Arterial pCO2 = Serum HCO3 + 15


===Role of the urine anion gap in the patient with a normal anion gap metabolic acidosis===
===Role of the Urine Anion Gap in the Patient with a Normal Anion Gap Metabolic Acidosis===
* [[Urine anion gap]] helps to differentiate [[renal tubular acidosis]]  (specifically a Type 1 or Type 4 RTA) from other causes of normal anion gap acidosis.   
* A [[urine anion gap]] helps to differentiate [[renal tubular acidosis]]  (specifically a Type 1 or Type 4 RTA) from other causes of normal anion gap acidosis.   
* The urine anion gap is calculated as the urine sodium plus urine potassium, minus the urine chloride
* The urine anion gap is calculated as the urine sodium plus urine potassium, minus the urine chloride
* Urine anion gap = (Urine Na + Urine K) - Urine Cl
* Urine anion gap = (Urine Na + Urine K) - Urine Cl
* The pathophysiology behind this is:
* The pathophysiology behind this is:
** When kidney is exposed to acidosis, the normal response of the kidney is to excrete acid.
** When the [[kidney]] is exposed to acidosis, the normal response of the kidney is to excrete acid.
** Kidney excretes the excess acid in the form of ammonium, NH4+.
** Kidney excretes the excess acid in the form of ammonium, NH4+.
**  To maintain neutrality, Cl- is excreted along with ammonium, NH4+.
**  To maintain neutrality, Cl- is excreted along with ammonium, NH4+.
** Thus, urine chloride act as a surrogate marker for urine ammonium (acidosis)
** Thus, urine chloride acts as a surrogate marker for urine ammonium (acidosis)
** In Types 1 and 4 renal tubular acidosis, the kidney's function of acid excretion is compromised (decreased excretion of NH4+ and Cl).
** In Types 1 and 4 renal tubular acidosis, the kidney's function of acid excretion is compromised (decreased excretion of NH4+ and Cl).
** Thus, in [[renal tubular acidosis]] (specifically a Type 1 or Type 4 RTA) urine anion gap will be high (> than zero).
** Thus, in [[renal tubular acidosis]] (specifically a Type 1 or Type 4 RTA) urine anion gap will be high (> than zero).
**  A urine anion gap less than zero in the normal anion gap metabolic acidosis suggests the kidney is excreting acid, making [[renal tubular acidosis]] less likely.
**  A urine anion gap less than zero in the normal anion gap metabolic acidosis suggests the kidney is excreting acid, making [[renal tubular acidosis]] less likely.
===Role of osmolar gap in differential diagnosis of elevated anion gap===
 
===Role of Osmolar Gap in Differential Diagnosis of Elevated Anion Gap===
* [[Methanol]], [[ethylene glycol]], [[isopropyl alcohol]], [[toluene]] are osmotically active substances.
* [[Methanol]], [[ethylene glycol]], [[isopropyl alcohol]], [[toluene]] are osmotically active substances.
* The estimated serum osmolality should be close to the actual, measured serum osmolality (within 10 points).
* The estimated serum osmolality should be close to the actual, measured serum osmolality (within 10 points).
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*** Presentation: [[Delirium]], [[papilledema]], and [[retinal hemorrhages]]
*** Presentation: [[Delirium]], [[papilledema]], and [[retinal hemorrhages]]
*** Elevated anion gap metabolic acidosis
*** Elevated anion gap metabolic acidosis
** '''Ethylene glycol'''
** '''Ethylene Glycol'''
*** Used in antifreeze and solvents
*** Used in antifreeze and solvents
*** Presentation: [[Delirium]]
*** Presentation: [[Delirium]]
*** Elevated anion gap metabolic acidosis
*** Elevated anion gap metabolic acidosis
*** Presence of '''oxalate crystals''' in urine
*** Presence of oxalate crystals in urine
** '''Isopropyl alcohol'''
** '''Isopropyl Alcohol'''
*** Also called rubbing alcohol
*** Also called rubbing alcohol
*** No acid-base disorder
*** No acid-base disorder
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** '''Toluene'''
** '''Toluene'''
*** Initial elevated anion gap followed with normal anion gap
*** Initial elevated anion gap followed with normal anion gap
* '''Estimated serum osmolality = (2 * serum sodium + BUN/2.8 + Glucose/18)'''
* Estimated serum osmolality = (2 * serum sodium + BUN/2.8 + Glucose/18)


===Buffer===
===Buffer===
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==References==
==References==
{{reflist|2}}
{{Reflist|2}}
 
[[Category:Needs overview]]
[[Category:Electrolyte disturbance]]
[[Category:Inborn errors of metabolism]]
[[Category:Medical tests]]
[[Category:Laboratory Test]]
[[Category:Nephrology]]
[[Category:Intensive care medicine]]
[[Category:Emergency medicine]]
 
{{WH}}
{{WH}}
{{WS}}
{{WS}}
[[Category:Disease]]
[[Category:Nephrology]]

Latest revision as of 22:34, 20 October 2014



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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Pathophysiology

Metabolic acidosis is the state of low blood pH that can result from:

  • Failure of the kidneys to excrete H+
  • Increased H+ load
  • Loss of bicarbonate

Shown below is a table summarizing the mechanisms of metabolic acidosis.

Mechanism Conditions
Failure to excrete H+

Decreased production of NH4+:

  • Renal failure
  • Renal tubular acidosis type 4 (hypoaldosteronism)

Decreased secretion of H+

  • Renal tubular acidosis type 1
Increased H+ load
  • Lactic acidosis
  • Ketoacidosis
  • Ingestions
  • Massive rhabdomyolysis
Loss of bicarbonate

Gastrointestinal loss of bicarbonates:

  • Diarrhea
  • Cholestyramine

Renal loss of bicarbonate:

  • Renal tubular acidosis type 2
  • Diuretics such as carbonic anhydrase inhibitors)

High Anion Gap Metabolic Acidosis

High anion gap metabolic acidosis can be caused by one of the following:

  • Lactic acidodis
  • Ketoacidosis
  • Renal failure
  • Ingestions

Lactic Acidosis

Ketoacidosis

Renal Failure

Ingestions

Compensatory Mechanisms

Metabolic acidosis is either due to increased generation of acid or an inability to generate sufficient bicarbonate. The body regulates the acidity of the blood by four buffering mechanisms.

Respiratory Compensation of Metabolic Acidosis

  • For 1 meq/L fall of serum HCO3 levels there is a 1.2 mmHg fall in arterial pCO2.
  • The respiratory compensation of metabolic acidosis is fast and begins within half an hour of metabolic acidosis.
  • In cases where the metabolic acidosis develops slowly, the respiratory compensation occurs simultaneously with the metabolic acidosis.
  • The respiratory compensation usually completes within 12 to 24 hours
  • A failure to develop adequate respiratory response indicates an acute underlying respiratory disease, neurologic disease or a very acute development of metabolic acidosis.
  • Formula for checking appropriate respiratory compensation to metabolic acidosis include:
    • Arterial pCO2 = 1.5 x serum HCO3- + 8 ± 2 (Winters' formula)
    • Arterial pCO2 = Serum HCO3 + 15

Role of the Urine Anion Gap in the Patient with a Normal Anion Gap Metabolic Acidosis

  • A urine anion gap helps to differentiate renal tubular acidosis (specifically a Type 1 or Type 4 RTA) from other causes of normal anion gap acidosis.
  • The urine anion gap is calculated as the urine sodium plus urine potassium, minus the urine chloride
  • Urine anion gap = (Urine Na + Urine K) - Urine Cl
  • The pathophysiology behind this is:
    • When the kidney is exposed to acidosis, the normal response of the kidney is to excrete acid.
    • Kidney excretes the excess acid in the form of ammonium, NH4+.
    • To maintain neutrality, Cl- is excreted along with ammonium, NH4+.
    • Thus, urine chloride acts as a surrogate marker for urine ammonium (acidosis)
    • In Types 1 and 4 renal tubular acidosis, the kidney's function of acid excretion is compromised (decreased excretion of NH4+ and Cl).
    • Thus, in renal tubular acidosis (specifically a Type 1 or Type 4 RTA) urine anion gap will be high (> than zero).
    • A urine anion gap less than zero in the normal anion gap metabolic acidosis suggests the kidney is excreting acid, making renal tubular acidosis less likely.

Role of Osmolar Gap in Differential Diagnosis of Elevated Anion Gap

  • Methanol, ethylene glycol, isopropyl alcohol, toluene are osmotically active substances.
  • The estimated serum osmolality should be close to the actual, measured serum osmolality (within 10 points).
  • If the measured serum osmolality is much higher (i.e. >10 points) than the estimated serum osmolality then presence of osmotically active substances should be suspected.
  • They can be differentiated because of these following characteristics:
    • Methanol
    • Ethylene Glycol
      • Used in antifreeze and solvents
      • Presentation: Delirium
      • Elevated anion gap metabolic acidosis
      • Presence of oxalate crystals in urine
    • Isopropyl Alcohol
      • Also called rubbing alcohol
      • No acid-base disorder
      • Metabolism causes increase acetone in the blood
      • Other conditions with elevated acetones in blood are: diabetes, starvation, and isopropyl alcohol.
    • Toluene
      • Initial elevated anion gap followed with normal anion gap
  • Estimated serum osmolality = (2 * serum sodium + BUN/2.8 + Glucose/18)

Buffer

  • The decreased bicarbonate that distinguishes metabolic acidosis is therefore due to two separate processes: the buffer (from water and carbon dioxide) and additional renal generation. The buffer reactions are: :H+ + HCO3- <--> H2CO3 <--> CO2 + H2O
  • The Henderson-Hasselbalch equation mathematically describes the relationship between blood pH and the components of the bicarbonate buffering system:
pH=pKa + log [HCO3-]/[CO2]
Using Henry's Law, we can say that [CO2]=0.03xPaCO2
(PaCO2 is the pressure of CO2 in arterial blood)
Adding the other normal values, we get
pH = 6.1 + log (24/0.03x40)
= 6.1 + 1.3
= 7.4

References

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